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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to investigate the mechanism of the "exaggerated natriuresis" in hypertension, 300 ml of 3% saline was infused for 1 hour during hydropenia in 13 patients with normal renin essential hypertension and 5 normotensive subjects on a daily ingestion of 4 Gm and 16 Gm of NaCl. At the end of the infusion, the circulating blood volume indicated by the change in serum total protein concentration and the glomerular filtered load were increased in a similar manner in both groups. Prompt the enhanced natriuresis and diuresis were seen within 1--2 hours after starting the infusion in the hypertensives on a daily ingestion of 16 Gm of NaCl. Significant positive correlations were found between the change in mean arterial blood pressure (deltaMAP) and UV, and between deltaMAP and UNa V in the hypertensives either on a daily 4 Gm or 16 Gm ingestion of NaCl. Free water reabsorption (Tc H2O) was lower in the hypertensives than that in the controls at high levels of osmolar clearance (Cosm). Plasma renin activity (PRA) did not differ in either group on either NaCl ingestion and was equally suppressed on a daily ingestion of 4 Gm of NaCl, while little changed on a high salt intake. Plasma aldosterone levels changed in parallel with PRA. It is suggested that the "exaggerated natriuresis" is due to the decreased tubular sodium reabsorption, which may be the result of intrarenal hemodynamic changes related to the elevated renal perfusion pressure. The decreased medullary osmolar gradient probably induced by an increase in the medullary blood flow is a possible contributing factor in the enhanced sodium and water excretion, and the renin-aldosterone system does not seem to play an important role.
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PMID:Sodium metabolism in essential hypertension. Natriuretic response to acute hypertonic saline load. 75 Jun 69

The basal levels of plasma norepinephrine have been measured in 113 carefully characterized patients with essential hypertension, and the results have been correlated with the PRA sub-grouping and the levels of blood pressure, plasma aldosterone, plasma 18-hydroxy-deoxycorticosterone, and plasma volume. In addition, the influence of furosemide on plasma norepinephrine concentration has been assessed. Essential hypertensives, when considered as a whole, did not exhibit any significant abnormality in basal plasma norepinephrine concentration, but interesting alterations were observed in certain specific sub-groups. High renin patients had significantly elevated levels of basal plasma norepinephrine. In addition, a sub-group of the low renin population who were relatively young had reduced plasma norepinephrine conentration. In these individuals with both reduced PRA and plasma norepinephrine, the levels of both increased concomitantly to the normal range with marked salt depletion. Furosemide administration induced increases in plasma norepinephrine in all PRA sub-groups. Plasma norepinephrine correlated significantly with blood pressure in normal and low renin hypertensives, but the relationships were confined only to male subjects. Significant correlations were also observed between plasma norepinephrine and plasma aldosterine in males with normal PRA but not in the other sub-categories. No significant relationships between plasma volume and either plasma norepinephrine or blood pressure could be detected. Plasma 18-hydroxy-deoxycorticosterone was greater in males as compared with females and appeared elevated above control levels in normal and high renin essential hypertensives. Significant positive correlations between plasma aldosterone and plasma 18-hydroxy-deoxycorticosterone were observed in both males and females with normal renin hypertension. These studies have demonstrated abnormalities in basal plasma norepinephrine concentration in certain patients with essential hypertension. They also suggest that the levels of blood pressure and plasma aldosterone may be related to peripheral sympathetic activity in essential hypertension.
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PMID:Relationship of basal plasma norepinephrine to blood pressure, plasma renin activity, mineralocorticoids, and plasma volume in essential hypertension. 75 99

The evidence supporting the thesis that hypertension can be prevented by eliminating salt from the diet is based on four principal sources: (1) epidemiological studies in unacculturated peoples showing that the prevalence of hypertension is inversely correlated with the degree of salt intake; (2) hemodynamic studies suggesting that the development of chronic experimental hypertension is a homeostatic response to a maintained increase in extracellular fluid volume (ECF); (3) evidence that the ECF of "salt eaters" is expanded in comparison to that of "no-salt eaters"; and (4) investigations in hypertensive patients receiving either diets greatly restricted in salt or continuous diuretic therapy which correlate the fall in blood pressure with a reduction in ECF. Although this mechanism of essential hypertension is still obscure the evidence is very good if not conclusive that reduction of salt in the diet to below 2 g/day would result in the prevention of essential hypertension and its disappearance as a major public health problem.
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PMID:Salt, volume and the prevention of hypertension. 76 20

The high sodium-low potassium environment of civilized people, operating on a genetic substrate of susceptibility, is the cardinal factor in the genesis and perpetuation of "essential" hypertension. The noxious effects begin in childhood, when habits of excess salt consumption are acquired at the family table, and are perpetuated by continuing habit and by increasing use of convenience and snack foods with artificially high concentrations of sodium and low levels of potassium. Present methods of food preparation leach out the protective potassium. Extradietary sodium chloride is a condiment not a requirement. Some primitive populations clearly preferred potassium chloride to sodium chloride. Chronic expansion of extracellular fluid volume induced by excess salt consumption causes the central and peripheral circulatory regulatory mechanisms to work at cross purposes, resulting in increased arterial pressure. The protective effect of potassium is dramatic and easily demonstrable in animals and man but its mechanism is not known. It cannot be entirely a direct effect on blood pressure because rats protected with extra potassium against a moderately high salt intake live much longer than control rats but have the same elevated blood pressures. In hypertension with a demonstrable "cause," the high sodium-low potassium environment makes a bad matter worse. In nature, feral man and his forebears were not confronted with excessive sodium and deficient potassium; indeed, the reverse was the case. Evolution has provided powerful mechanisms for conserving sodium and eliminating potassium, but no efficient physiologic mechanisms for conserving potassium and eliminating excess sodium. Most laboratory animal "control" diets contain an amount of sodium that fully suppresses aldosterone secretion, and the same is true of the "average" diet of the American people. Inadequate attention to dietary sodium and potassium makes many studies in both animals and man of uncertain validity. Internally, essential hypertension is an exceedingly complex mosaic of physiologic interactions. Viewed from outside, it is a disorder for which genetic material sets the stage; excessive sodium precipitates it and perpetuates it. Extra salt makes all forms more rapidly progressive and accelerates the onset of terminal events; extra potassium is everywhere protective. When an entire population eats excessively of salt, hypertension will develop among those genetically susceptible, but epidemiologic studies of salt versus blood pressure will not show a relation of salt to hypertension. This is the saturation effect. Low sodium diets are therapeutically effective but generally regarded as an impossible or an unnecessary nuisance. Effective prevention programs must be instituted at as early an age as possible. The efficacy of a prophylactic/therapeutic low sodium-high potassium diet should be weighed against the uncertain hazards of a lifetime of pill taking.
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PMID:High sodium-low potassium environment and hypertension. 79 67

Hemodynamics and plasma renin activity were measured in 20 ambulatory hospital inpatients with untreated mild to moderate essential hypertension. The control measurements were made after a period of four to seven days just on a diet containing 10 mEq sodium per day. The measurements were repeated following a week of oral propranolol hydrochloride therapy plus the low salt diet. Heart rate (P less than .001), mean arterial pressure (P less than .001), cardiac output (P less than .05), and plasma renin activity (P less than .05) were reduced in the majority of these patients following propranolol therapy but stroke volume increased (P less than .05). Corrected ejection time and total peripheral resistance did not show significant change. The antihypertensive effect of propranolol could not be related to its hyporeninemic effect or to the fall in cardiac output. Under the experimental conditions of this study, no single parameter, either hemodynamic or plasma renin activity, was predictive of a definite antihypertensive response to propranolol therapy.
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PMID:Hemodynamic and plasma renin effects of propranolol in essential hypertension. 84 47

Previous studies have reported an exaggerated natriuresis in hypertensive man; however, a systematic appraisal of this response in various forms of hypertension has not been made. We measured fractional excretion of sodium (FENa) during a four hour intravenous infusion of 2 liters normal saline in 162 normal subjects and 120 hypertensives. Of these, 13 had primary aldosteronism (ALDO), 19 high renin (HRH), 30 low renin (LRH), and 57 normal renin (NRH) essential hypertension. FENa for normals (1.42%), NRH (1.57%), and HRH (1.46%) was similar. That for LRH (2.56%) and ALDO (4.18%) was elevated compared to the other three subgroups (P less than 0.001). Although the four hour FENa during saline infusion was associated with mean atrterial blood pressure (MABP) within the entire hypertensive population (r = 0.51), when the subgroups of the hypertensive patients were considered separately no association between FENa and MABP was identified. Moreover, the MABP of subjects with HRH was greater (P less than 0.05) than in those with NRH, although the FENa of the two subgroups was similar. Patients with ALDO and LRH have a greater natriuretic response to a salt load than do other subgroups of essential hypertension or normal subjects. The exaggerated natriuresis appears to be a feature of hypertension with renin suppression. The degree of exaggerated natriuresis in not solely a function of an elevated mean arterial blood pressure.
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PMID:Natriuretic response to saline infusion in normotensive and hypertensive man. The role of renin suppression in exaggerated natriuresis. 84 36

In order to investigate a role of sympathetic nervous system in the mechanism of blood-pressure elevation in essential hypertension, urinary catecholamines, serum dopamine-beta-hydroxylase (DBH) activity and a pressor response to infused noradrenaline (noradrenaline response) were measured, in the patients with essential hypertension, before and 2 weeks-rest after hospitalization or following salt restriction. In addition, plasma renin activity (PRA) and water-sodium contents were determined and a correlation between these variables and noradrenaline excretion, serum DBH or noradrenaline response was observed. A blood pressure fall after hospitalization was associated with a decrease of urinary noradrenaline and serum DBH, and there was a significantly positive correlation between the changes in blood pressure and those in urinary noradrenaline or in serum DBH. A significantly adverse correlation was found between plasma volume and the amounts of urinary noradrenaline excretion. The changes in noradrenaline response was negatively correlated with those in urinary noradrenaline excretion. In addition, noradrenaline response was correlated positively with plasma volume, extracellular fluid volume and total exchangeable sodium and negatively with PRA. Following salt restriction, a fall of the blood pressure was associated with an elevation of urinary noradrenaline excretion. The patients with more marked blood pressure fall showed a higher increase of urinary noradrenaline, and a significant correlation was found between the changes in these two variables. Noradrenaline response was significantly reduced, although it was not correlated significantly with noradrenaline excretion. In these experiments, adrenaline, unlike noradrenaline, did not show any obvious changes. These findings suggested that an excessive sympathetic nerve activity caused an elevation of blood pressure in the labile type of essential hypertension. It was demonstrated that a sympathetic nervous function was dependent on sodium intake and that there exisited a close relationship between noradrenaline response and water-sodium contents or PRA.
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PMID:Studies on the role of sympathetic nervous system in the mechanism of essential hypertension. 87 Jul 20

Hypertension in spontaneously hypertensive rats (SHR) develops initially without any obvious organic lesions, and mainly with hemodynamic alteration due to increased peripheral vascular resistance. It is then followed later by various cardiovascular complications such as stroke. These facts indicate that this spontaneous hypertension is very similar to essential hypertension in man. Studies on the pathogenic mechanisms of spontaneous hypertension up to the present have revealed the following points. (1) This hypertension is genetically transmitted to the offspring in an additive mode by a relatively small number of major genes; (2) Environmental factors such as stress and salt-loading accelerate the hypertension; (3) Parabiosis between SHR and normotensive rats offered no positive evidence indicating the involvement of any strong humoral factors; (4) Assays on adrenal and thyroid hormones have suggested that this hypertension is not a simple endocrine hypertension; (5) The destruction of the central nervous system or sympathectomy on blood pressure or peripheral vascular resistance, as well as the recording of spontaneous sympathetic discharge, etc. have indicated the positive involvement of the autonomic nervous system in the development of this hypertension; (6) Changes in the enzyme activities of the central nervous system and in the central responses to various candidates of central neurotransmitters suggested that 'noradrenergic inhibitory mechanisms for blood pressure regulation in the brainstem' (Yamori, Lovenberg and Sjoerdsma, 1970) might be insufficient and result in the initial enhancement of peripheral vasomotor tone causing labile hypertension; (7) Noradrenalin turnover study of the heart and hindlimb perfusion experiments indicated that the neural factor was mainly involved in the development or the early stage of hypertension; this finding was further supported by the increased noradrenalin level or dopamine-beta-hydroxylase activity in the blood; (8) Histometrical studies indicated that the structural component of the peripheral vascular resistance stabilized the hypertension; (9) The initial neurogenic factors and successive involvement of nonneurogenic factors are relayed by the acceleration of protein metabolism of the vascular wall ('adaptive metabolic change', Yamori, 1974). This acceleration is commonly detected by amino acid incorporation study in both spontaneous and other experimental hypertension; (10) Increased lysine incorporation into the noncollagenous protein of the mesenteric arteries detected in the prehypertensive SHR was experimentally confirmed to be influenced by neural innervation. This confirmation indicated the importance of such a trophic effect of the nervous system on the structural alteration of blood vessels in the development of hypertension (neurovascular linkage, Yamori, 1975)...
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PMID:Pathogenesis of spontaneous hypertension as a model for essential hypertension. 87 Jul 22

The relationship between urinary kallikrein, urinary aldosterone, and plasma renin activity (PRA) was studied in hypertensive patients and normal subjects. Kallikrein was measured by a radiochemical esterolytic assay. Nine white males with normal renin, mild essential hypertension (25 +/- 5 [SD] yr; blood pressure [BP] 143 +/- 7 / 95 +/- 5 mm Hg) and six white normal males (23 +/- 3 yr; BP 115 +/- 15 / 70 +/- 6 mm Hg) were placed on a one-week diet consisting of 400 mEq Na+, 80 mEq K+ diet and a one week diet of a 10 mEq Na+, 80 mEq K+ diet. During salt restriction, PRA, urinary aldosterone, and urinary kallikrein progressively rose. (Urinary kallikrein on day 7: normals 18.3 +/- 13.7 esterase units [EU] per 24 hr; hypertensives 22.7 +/- 12.5 EU/24 hrs). There were no significant differences between the normals and hypertensives in PRA, aldosterone, or kallikrein excretion. After sodium balance was achieved, during salt loading, the PRA, aldosterone and kallikrein values were similar in both normals and hypertensives. (Urinary kallikrein on day 7: normals 5.0 +/- 5.2; hypertensives 7.9 +/- 4.4 EU/24 hrs.) Abnormalities in urinary kallikrein in hypertensives were not found when young white males with normal renin essential hypertension were compared to age-matched white male normal subjects. PRA appears related to urinary kallikrein excretion in this type of patient.
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PMID:Urinary kallikrein in normal renin essential hypertension. 91 48

Serial measurements of plasma-prolactin concentration (HPr) and plasma-renin activity (PRA) at 30-min intervals were made in 19 male patients with essential hypertension and in 8 normotensive subjects. HPr was markedly higher in the hypertensive patients than in the normotensive controls. Patients with reduced plasma-renin activity and only slightly elevated HPr-levels showed lower urinary sodium excretion, but a more pronouced 24-h natriuretic response to i.v. furosemide than patients with normal renin and very high HPr-levels. Six patients were treated with the dopaminergic agonist bromocriptine. The drug induced a significant blood pressure reduction in five patients and normalised pressure in two patients. The data do not indicate a role for prolactin in sustaining hypertension via renal salt retaining mechanisms. It is suggested that the raised HPr-levels represent an index of altered central nervous function, characterized by reduced hypothalamic activity. The blood pressure-lowering effect of the dopaminergic agonist bromocriptine fits with the hypothesis that reduced hypothalamic dopaminergic activity might be a factor in the pathogenesis of essential hypertension.
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PMID:[Raised plasma-prolactin levels in essential hypertension: index of reduced hypothalamic dopaminergic activity (author's transl)]. 92 11


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